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Insulin resistance (IR) is a putative risk factor for cognitive decline and dementia, and has been shown to impede neuronal
glucose metabolism in animal models. This post-hoc study focused on metabolic changes in the medial prefrontal region,
a brain region exhibiting decline years before documented cognitive changes, relative to high or low IR status in a cohort
of postmenopausal women at risk for dementia who were randomized to continue or discontinue existing stable hormone
therapy (HT) for 2 years. Subjects were dichotomized into high and low IR groups based on the homeostatic model assessment
of insulin resistance, which was within clinically normal limits for the group as a whole at both baseline and 2-year followup.
Results showed that high and low IR groups showed significant differences in metabolic decline of the medial prefrontal
gyrus, regardless of HT randomization group. However, HT randomization was predictive of metabolic decline only in women
with low HOMA. Performance in working memory was consistent with observed metabolic changes. These results suggest IR
may be an independent moderator of regional metabolic changes, while protective metabolic effects of HT are most apparent
in those at low-end range of IR. If replicated in future studies, these findings will help to better understand the interaction
between putative risk and protective factors, and further delineate cohort postmenopausal women who may benefit from HT.
Biography
Natalie Rasgon received her MD and PhD in Obstetrics and Gynecology and Pathological Physiology in the USSR, she began her distinguished career at UCLA
School of Medicine, and in 2002, she established the Center for Neuroscience in Women�s Health at Stanford. She is the author of more than 130 peer-reviewed
publications, 25 book chapters, and is a reviewer for 30 professional journals. Her predominant research focus has been on the treatment of bipolar disorder in
women, the use of hormonal interventions during menopause and the effects on mood and cognitive function, and the interplay between endocrine function and
aging.
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